Pallavi Ghosh

Pallavi Ghosh, Ph.D.

Mycobacterial Stress Response
Ph.D. Center for Cellular & Molecular Biology, Hyderabad, India
Postdoctoral training: University of Pittsburgh

Research Interests

Mycobacterium abscessus (Mab) is a rapidly growing environmental species of mycobacteria. It causes skin and soft tissue infections post trauma and surgery as well as broncho-pulmonary infection and acute respiratory failure in patients with chronic lung damage. Cystic fibrosis (CF) patients are particularly vulnerable to Mab infections. Cure rates are deplorably low (~50%), involving 6-12 month long regimens of multiple, often noxious, antibiotics and/or, surgical resection.

Mycobacterium abscessus infections are incredibly difficult to treat due to three primary reasons:

  1. Mab is highly resistant to most FDA approved antibiotics such as rifampicin, isoniazid, ethambutol, tetracyclines and streptomycin, making them unavailable for therapy.
  2. Mab displays initial susceptibility to some antibiotics (e.g. macrolides) but becomes resistant after extending the testing period. Exposure to antibiotics induces transcription of drug resistance genes resulting in delayed resistance.
  3. There is a poor correlation between in vitro antibiotic susceptibility and in vivo efficacy, a part of which may be attributed to the ability of Mab to form biofilms.

The primary focus of the lab is to decipher the molecular mechanisms involved in the extreme drug resistance of Mycobacterium abscessus.

Specific projects include:

  1. Systems level understanding of changes that accompany exposure of M. abscessus to antibiotics.
  2. Identification of effectors that confer unique profiles of drug resistance.
  3. Screening of small molecule libraries for inhibitors of identified targets.
  4. Study the role of biofilm formation on antibiotic resistance of M. abscessus.

We use a combination of bacterial genetics, biochemistry and high throughput genomic analysis to decipher mechanisms of drug resistance.

To learn more, please visit the Ghosh Laboratory.

Select Publications
Hurst-Hess K, Walz A, Yang Y, McGuirk H, Gonzalez-Juarrero M, Hatfull GF, Ghosh P, Ojha AK. Intrapulmonary Treatment with Mycobacteriophage LysB Rapidly Reduces Mycobacterium abscessus Burden. Antimicrob Agents Chemother. 2023; May (8:e0016223): DOI: 10.1128/aac.00162-23
Hurst-Hess K, McManaman C, Yang Y, Gupta S, Ghosh P. Hierarchy and networks in the transcriptional response of Mycobacterium abscessus to antibiotics. bioRxiv. 2023; Mar 17 (03.16.533064): DOI: 10.1101/2023.03.16.533064
Hurst-Hess KR, Phelps GA, Wilt LA, Lee RE, Ghosh P. Mab2780c, a TetV-like efflux pump, confers high-level spectinomycin resistance in mycobacterium abscessus. Tuberculosis (Edinb). 2023; Jan (138): 102295. DOI: 10.1016/
Hurst-Hess KR, Saxena A, Rudra P, Yang Y, Ghosh P. Mycobacterium abscessus HelR interacts with RNA polymerase to confer intrinsic rifamycin resistance. Mol Cell. 2022; 82 (17): 3166-77.e5. DOI: 10.1016/j.molcel.2022.06.034
Hurst-Hess KR, Rudra P, Ghosh P. Ribosome Protection as a Mechanism of Lincosamide Resistance in Mycobacterium abscessus. Antimicrob Agents Chemother. 2021; 65 (11): e0118421. DOI: 10.1128/AAC.01184-21
Rudra P, Hurst-Hess KR, Cotten KL, Partida-Miranda A, Ghosh P. Mycobacterial HflX is a ribosome splitting factor that mediates antibiotic resistance. Proc Natl Acad Sci U S A. 2020; 117 (1): 629-634. DOI: 10.1073/pnas.1906748117
Hurst-Hess K, Biswas R, Yang Y, Rudra P, Lasek-Nesselquist E, Ghosh P. Mycobacterial SigA and SigB Cotranscribe Essential Housekeeping Genes during Exponential Growth. mBio. 2019; 10 (3): e00273-19. DOI: 10.1128/mBio.00273-19
Rudra P, Hurst-Hess K, Lappierre P, Ghosh P. High Levels of Intrinsic Tetracycline Resistance in Mycobacterium abscessus Are Conferred by a Tetracycline-Modifying Monooxygenase. Antimicrob Agents Chemother. 2018; 62 (6): e00119-18. DOI: 10.1128/AAC.00119-18
Hurst-Hess K, Rudra P, Ghosh P. Mycobacterium abscessus WhiB7 Regulates a Species-Specific Repertoire of Genes To Confer Extreme Antibiotic Resistance. Antimicrob Agents Chemother. 2017; 61 (11): e01347-17. DOI: 10.1128/AAC.01347-17
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